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Tabbó F, Barreca A, Piva R, et al. ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma. Front Oncol. 2012;2:41doi: 10.3389/fonc.2012.00041.
Tabbó, F., Barreca, A., Piva, R., Inghirami, G. (2012). ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma. Frontiers in oncology, 241. https://doi.org/10.3389/fonc.2012.00041
Tabbó, Fabrizio, et al. "ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma." Frontiers in oncology vol. 2 (2012): 41. doi: https://doi.org/10.3389/fonc.2012.00041
Tabbó F, Barreca A, Piva R, Inghirami G. ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma. Front Oncol. 2012 May 11;2:41. doi: 10.3389/fonc.2012.00041. eCollection 2012. PMID: 22649787; PMCID: PMC3355932.
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Front Oncol. 2012 May 11;2:41. doi: 10.3389/fonc.2012.00041. eCollection 2012.

ALK Signaling and Target Therapy in Anaplastic Large Cell Lymphoma.

Frontiers in oncology

Fabrizio Tabbó, Antonella Barreca, Roberto Piva, Giorgio Inghirami,

Affiliations

  1. Department of Pathology, Center for Experimental Research and Medical Studies, University of Torino Torino, Italy.

PMID: 22649787 PMCID: PMC3355932 DOI: 10.3389/fonc.2012.00041

Abstract

The discovery by Morris et al. (1994) of the genes contributing to the t(2;5)(p23;q35) translocation has laid the foundation for a molecular based recognition of anaplastic large cell lymphoma and highlighted the need for a further stratification of T-cell neoplasia. Likewise the detection of anaplastic lymphoma kinase (ALK) genetic lesions among many human cancers has defined unique subsets of cancer patients, providing new opportunities for innovative therapeutic interventions. The objective of this review is to appraise the molecular mechanisms driving ALK-mediated transformation, and to maintain the neoplastic phenotype. The understanding of these events will allow the design and implementation of novel tailored strategies for a well-defined subset of cancer patients.

Keywords: anaplastic large cell lymphoma; anaplastic lymphoma kinase; chimeric fusion proteins; molecular targeted therapy; signaling pathways

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